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High Altitude Pulmonary Edema
Classification and external resources
ICD-10 T702
ICD-9 993.2

High altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema (fluid accumulation in the lungs) that occurs in otherwise healthy mountaineers at altitudes typically above 2,500 meters (Template:Convert/ft)Template:Convert/test/A.[1] Some cases, however, have been reported also at lower altitudes (between Template:Convert/-Template:Convert/test/A in highly vulnerable subjects), although what makes some people susceptible to HAPE is not currently known. HAPE remains the major cause of death related to high-altitude exposure with a high mortality in absence of adequate emergency treatmentTemplate:POV-statement.

Symptoms[edit | edit source]

Physiological and symptomatic changes often vary according to the altitude involved.[2]

The Lake Louise Consensus Definition for High Altitude Pulmonary Edema has set widely-used criteria for defining HAPE symptoms: [3][4]

Symptoms: at least two of:

  • Difficulty in breathing (dyspnea) at rest
  • Cough
  • Weakness or decreased exercise performance
  • Chest tightness or congestion

Signs: at least two of:

  • Crackles or wheezing (while breathing) in at least one lung field
  • Central cyanosis (blue skin color)
  • Tachypnea (rapid shallow breathing)
  • Tachycardia (rapid heartrate)
Intermediate Altitudes (1500-2500 m or 4900-8200 feet)

Clinical symptoms are unlikely. Blood oxygen levels remain >90%.

High Altitude (2500-3500 m or 8200-11500 feet)

Clinical symptoms are common and may develop after 2-3 days. Blood oxygen levels may drop below 90% or lower during exercise. Prior acclimatisation will decrease the severity of the symptoms.

Extreme Altitude (>5800 m or 19000 feet)

Blood oxygen levels are <90%, even at rest. Progressive deterioration may occur despite acclimatisation.

Causes[edit | edit source]

The initial cause of HAPE is a shortage of oxygen which is caused by the lower air pressure at high altitudes.[1][5] The mechanisms by which this shortage of oxygen causes HAPE are poorly understood, but two processes are believed to be important:

  1. Increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction.[6]
  2. An idiopathic non-inflammatory increase in the permeability of the vascular endothelium.[7]

Although higher pulmonary arterial pressures are associated with the development of HAPE, the presence of pulmonary hypertension may not in itself be sufficient to explain the development of edema: severe pulmonary hypertension can exist in the absence of clinical HAPE in subjects at high altitude.[8]

Incidence[edit | edit source]

The incidence of clinical HAPE in unacclimatized travelers exposed to high altitude (~Template:Convert/LoffAonDorSoffTemplate:Convert/test/Aon) appears to be less than 1%.[citation needed] The U.S. Army Pike's Peak Research Laboratory has exposed sea-level-resident volunteers rapidly and directly to high altitude; during 30 years of research involving about 300 volunteers (and over 100 staff members), only three have been evacuated with suspected HAPE[citation needed].

Predisposing factors[edit | edit source]

Individual susceptibility to HAPE is difficult to predict. The most reliable risk factor is previous susceptibility to HAPE, and there is likely to be a genetic basis to this condition, perhaps involving the gene for angiotensin converting enzyme (ACE).[citation needed] Recently, scientists have found the similarities between low amounts of 2,3-BPG (also known as 2,3-DPG) with the occurrence of HAPE at high altitudes.[citation needed]

Research[edit | edit source]

In order to help understand the factors that make some individuals susceptible to HAPE, the International HAPE Database was set up in 2004.[9] Individuals who have previously suffered from HAPE can register with this confidential database in order to help researchers study the condition.

Treatment[edit | edit source]

The standard and most important treatment is to descend to lower altitude as quickly as possible, preferably by at least 1000 metres.[1][10] Oxygen should also be given if possible. Symptoms tend to quickly improve with descent, but less severe symptoms may continue for several days. The standard drug treatments for which there is strong clinical evidence are dexamethasone.[11] and nifedipine[12] Phosphodiesterase inhibitors such as tadalafil are also effective[11] but may worsen the headache of mountain sickness.[13]

See also[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 1.2 (2002) "High-Altitude Pulmonary Edema" Medical Aspects of Harsh Environments, 789–814. URL accessed 2009-01-05.
  3. "Lake Louise Consensus on the Definition of Altitude Illness", ISMM, August 2001, webpage: ISMM-LL.
  5. Kenneth Baillie and Alistair Simpson. Barometric pressure calculator. Apex (Altitude Physiology EXpeditions). URL accessed on 2006-08-10. - Online altitude calculator
  6. Bärtsch P, Maggiorini M, Ritter M, Noti C, Vock P, Oelz O (October 1991). Prevention of high-altitude pulmonary edema by nifedipine. The New England Journal of Medicine 325 (18): 1284–9.
  7. Swenson ER, Maggiorini M, Mongovin S, et al. (May 2002). Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor. JAMA 287 (17): 2228–35.
  8. Maggiorini M, Mélot C, Pierre S, et al. (April 2001). High-altitude pulmonary edema is initially caused by an increase in capillary pressure. Circulation 103 (16): 2078–83.
  9. International HAPE database. Apex (Altitude Physiology EXpeditions). URL accessed on 2006-08-10.
  10. Luks AM (2008). Do we have a 'best practice' for treating high altitude pulmonary edema?. High Altitude Medicine & Biology 9 (2): 111–4.
  11. 11.0 11.1 Maggiorini M, Brunner-La Rocca HP, Peth S, et al. (October 2006). Both tadalafil and dexamethasone may reduce the incidence of high-altitude pulmonary edema: a randomized trial. Annals of Internal Medicine 145 (7): 497–506.
  12. Bärtsch P, Swenson ER, Maggiorini M (2001). Update: High altitude pulmonary edema. Advances in Experimental Medicine and Biology 502: 89–106.
  13. Bates MG, Thompson AA, Baillie JK (March 2007). Phosphodiesterase type 5 inhibitors in the treatment and prevention of high altitude pulmonary edema. Current Opinion in Investigational Drugs 8 (3): 226–31.

External links[edit | edit source]

Template:Consequences of external causes

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